The Lyme Disease Debate Host Biodiversity and Human Disease Risk

Abstract

In the mid-1970s, several children in the town of Lyme, Connecticut, began to suffer from painful, swollen joints. They were diagnosed with juvenile rheumatoid arthritis, a rare condition. Clinicians at Yale School of Medicine suspected the cluster of cases was caused by an infectious agent.1 The illness, dubbed Lyme disease, was soon recorded in an increasing number of patients in the northeastern United States. Symptoms included rashes, fevers, joint and muscle pain, and heart and neurological problems. National Institutes of Health researcher Willy Burgdorfer identified the culprit in 1982: a spirochete bacterium that, in electron micrograph images, resembles a broken twist of barbed wire.2 The spirochete, named Borrelia burgdorferi (Bb), was first isolated from the gut of ticks collected in woodlands on Shelter Island, New York, where Lyme disease had become endemic. The deer tick (Ixodes scapularis) transmits the bacterium Borrelia burgdorfi (Bb) to humans in the course of one of three blood meals it will take in its lifetime. Thirty years after its discovery, Lyme disease has become by far the most common vectorborne infection in North America.3 Today the ecology of Bb is the subject of both intense study and intense scientific debate. Some researchers think that protecting large tracts of forest habitat—a strategy that increases the diversity of vertebrate hosts for both Bb and its tick vectors—will ultimately reduce the risk of human infection. Others argue that there is no predictable relationship between host biodiversity and human disease risk.